Mìžnarodnij Endokrinologìčnij Žurnal (Mar 2022)
Dynamics of endocrine and metabolic changes among patients with coronary artery disease, type 2 diabetes mellitus and metabolic syndrome while treating with telmisartan
Abstract
Background. The correlation between renin-angiotensin system and hypothalamic-pituitary system is a pathogenetic link leading to many comorbid diseases, particularly type 2 diabetes mellitus (DM) and coronary artery disease (CAD). Several studies have been dedicated to the hormones of the pituitary gland, hypothalamus as well as peripheral organs of the endocrine system. The presence of common links between pathogenesis and regulating factors forces us to search for new methods of treatment which should have an overall effect on comorbid diseases. The use of telmisartan, which is a blocker of angiotensin II receptors, is among various treatment options. Nevertheless, the changes in hormonal status and lipid spectrum, which are characteristic of the patient’s condition in the course of treatment, remain to be insufficiently researched. This is the reason that justifies the expediency of our research. The study is aimed at scrutinizing the dynamics of endocrine and metabolic changes in patients suffering from coronary artery disease, type 2 diabetes mellitus caused by metabolic syndrome (MS) while treating with telmisartan. Materials and methods. Fifty-one patients (26 female and 25 male patients) suffering from coronary artery disease and type 2 diabetes mellitus triggered by metabolic syndrome were examined in Lviv Regional State Clinical Medical Treatment and Diagnostic Endocrinology Center and CNE “City Clinical Hospital 5 in Lviv”. The patients were divided into two groups: experimental group and comparison group depending on the treatment prescribed. The experimental group consisted of patients (n = 27) suffering from CAD, type 2 DM and MS (women — 14, men — 13) who were prescribed with telmisartan 80 mg/day and standard therapy. The comparison group consisted of 24 patients with CAD and type 2 DM caused by MS (women — 12, men — 12) who were prescribed with standard therapy. The control group consisted of 40 healthy individuals (men — 17 (42.5 %), women — 23 (57.5 %)). The first examination was conducted on admission to an inpatient department and the second one was performed in a month after the beginning of treatment. Patients’ levels of prolactin, cortisol, free thyroxine, and thyroid-stimulating hormone as well as lipid spectrum parameters were defined. Results. The dynamics of the changes of prolactin, cortisol, free thyroxine, and thyroid-stimulating hormone levels in patients suffering from CAD, type 2 DM caused by MS was studied before and a month after the start of treatment with telmisartan. The results of the study demonstrated the changes in hormonal spectrum and lipid metabolism after the beginning of treatment with telmisartan. The cortisol level in the experimental group was not significantly different from the control values on admission to the inpatient department. Within a month of treatment, the cortisol level exhibited a tendency to decrease in comparison with its initial level. The cortisol level in the comparison group also tended to reduce in standard therapy if compared to its initial level. Therefore, both treatment with Telmisartan and standard therapy contributed to the reduction of the cortisol level. Before the start of treatment in the inpatient department, the prolactin level in women of the experimental group was not significantly different from the control values and kept increasing substantially within a month of treatment, whereas the prolactin level in females of the comparison group exhibited only a growing tendency within the course of treatment. At the beginning of observation, the prolactin level in men of the experimental group was significantly higher than the control values. While treating with telmisartan, the level of prolactin in males of the experimental group increased significantly, whereas in the comparison group, it did not change dramatically. Therefore, a considerable increase of prolactin levels in males and females was observed in telmisartan treatment. The level of thyroid-stimulating hormone in patients of the experimental group was significantly higher if compared with the control values before the beginning of treatment. The level of the above-mentioned hormone kept decreasing considerably within the course of treatment unlike the thyroid-stimulating hormone level in patients of the comparison group which tended to increase at the beginning of observation and did not change dramatically in the course of treatment. The major increase in free thyroxine level was typical for the patients in the experimental group within the course of treatment, while the level of free thyroxine in the patients of the comparison group did not change significantly in the course of treatment. A dramatic increase in levels of triglycerides as well as very-low density lipoprotein cholesterol and a significant decrease in high-density lipoprotein cholesterol were typical for the lipid spectrum in patients of both experimental and comparison groups. The use of telmisartan as a part of standard therapy was accompanied by a significant decrease in total cholesterol (within the reference values), triglycerides, low density lipoprotein cholesterol and very-low density lipoprotein cholesterol. Conclusions. The use of telmisartan as a part of combined therapy facilitates the reduction of the cortisol level (p > 0.05) and leads to a significant rise in male and female prolactin levels (within the range of reference values). It triggers an apparent increase in free thyroxine and decrease in thyroid-stimulating hormone. These findings reveal the impact of telmisartan on the correction of metabolic disorders, particularly the effect on the manifestations of subclinical hypothyroidism. Telmisartan has a beneficial effect on the lipid spectrum of blood. It greatly reduces the levels of total cholesterol, triglycerides, low density lipoprotein cholesterol as well as very-low density lipoprotein cholesterol.
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